The lung and the gut: Common origins, close links

Girosi, Donata; Bellodi, Simona; Sabatini, Federica; Rossi, Giovanni A.

doi:10.1016/j.prrv.2006.04.192

Cited by 23 publications

(14 citation statements)

References 24 publications

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“…The molecular basis of fetal lung development is believed to be under genetic and hormonal control [ 47 , 48 ]. Molecular cloning studies have shown that CFTR gene expression is regulated during lung development [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Transient in utero disruption of Cystic Fibrosis Transmembrane Conductance Regulator causes phenotypic changes in Alveolar Type II cells in adult rats

et al. 2009

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BackgroundMechanicosensory mechanisms regulate cell differentiation during lung organogenesis. We have previously demonstrated that cystic fibrosis transmembrane conductance regulator (CFTR) was integral to stretch-induced growth and development and that transient expression of antisense-CFTR (ASCFTR) had negative effects on lung structure and function. In this study, we examined adult alveolar type II (ATII) cell phenotype after transient knock down of CFTR by adenovirus-directed in utero expression of ASCFTR in the fetal lung.ResultsIn comparison to (reporter gene-treated) Controls, ASCFTR-treated adult rat lungs showed elevated phosphatidylcholine (PC) levels in the large but not in the small aggregates of alveolar surfactant. The lung mRNA levels for SP-A and SP-B were lower in the ASCFTR rats. The basal PC secretion in ATII cells was similar in the two groups. However, compared to Control ATII cells, the cells in ASCFTR group showed higher PC secretion with ATP or phorbol myristate acetate. The cell PC pool was also larger in the ASCFTR group. Thus, the increased surfactant secretion in ATII cells could cause higher PC levels in large aggregates of surfactant. In freshly isolated ATII cells, the expression of surfactant proteins was unchanged, suggesting that the lungs of ASCFTR rats contained fewer ATII cells. Gene array analysis of RNA of freshly isolated ATII cells from these lungs showed altered expression of several genes including elevated expression of two calcium-related genes, Ca2+-ATPase and calcium-calmodulin kinase kinase1 (CaMkk1), which was confirmed by real-time PCR. Western blot analysis showed increased expression of calmodulin kinase I, which is activated following phosphorylation by CaMkk1. Although increased expression of calcium regulating genes would argue in favor of Ca2+-dependent mechanisms increasing surfactant secretion, we cannot exclude contribution of alternate mechanisms because of other phenotypic changes in ATII cells of the ASCFTR group.ConclusionDevelopmental changes due to transient disruption of CFTR in fetal lung reflect in altered ATII cell phenotype in the adult life.

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Section: Discussionmentioning

confidence: 99%

Transient in utero disruption of Cystic Fibrosis Transmembrane Conductance Regulator causes phenotypic changes in Alveolar Type II cells in adult rats

et al. 2009

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“…The epithelium of the respiratory and gastrointestinal systems are derived embryonically from the primitive foregut ( 1 ). This shared origin likely underlies the ability of these two mucosal surfaces to act similarly as selective barriers, allowing for the translocation of gases or nutrients, whilst maintaining mutualistic relationships with the microbiota and keeping pathogens at bay.…”

Section: Chronic Inflammatory Diseasesmentioning

confidence: 99%

“…Inflammatory bowel disease (IBD) and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases that affect the gastrointestinal tract and respiratory system, respectively, with both being characterized by recurrent disease cycles that result in tissue damage and worsening of disease symptoms. As mucosal epithelial sites, the gastrointestinal and respiratory tracts share structural similarities which may result in part from common embryonic origin in the primitive foregut (1). Its hypothesized that these structural similarities may account for inherent parallels in the immune responses at these two sites and contribute to the dynamic involvement of the gut-lung axis in inflammation.…”

Section: Introductionmentioning

confidence: 99%

Links Between Inflammatory Bowel Disease and Chronic Obstructive Pulmonary Disease

et al. 2020

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Inflammatory bowel disease (IBD) and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases of the gastrointestinal and respiratory tracts, respectively. These mucosal tissues bear commonalities in embryology, structure and physiology. Inherent similarities in immune responses at the two sites, as well as overlapping environmental risk factors, help to explain the increase in prevalence of IBD amongst COPD patients. Over the past decade, a tremendous amount of research has been conducted to define the microbiological makeup of the intestine, known as the intestinal microbiota, and determine its contribution to health and disease. Intestinal microbial dysbiosis is now known to be associated with IBD where it impacts upon intestinal epithelial barrier integrity and leads to augmented immune responses and the perpetuation of chronic inflammation. While much less is known about the lung microbiota, like the intestine, it has its own distinct, diverse microflora, with dysbiosis being reported in respiratory disease settings such as COPD. Recent research has begun to delineate the interaction or crosstalk between the lung and the intestine and how this may influence, or be influenced by, the microbiota. It is now known that microbial products and metabolites can be transferred from the intestine to the lung via the bloodstream, providing a mechanism for communication. While recent studies indicate that intestinal microbiota can influence respiratory health, intestinal dysbiosis in COPD has not yet been described although it is anticipated since factors that lead to dysbiosis are similarly associated with COPD. This review will focus on the gut-lung axis in the context of IBD and COPD, highlighting the role of environmental and genetic factors and the impact of microbial dysbiosis on chronic inflammation in the intestinal tract and lung.

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“…In our case, the association of esophageal duplication cyst with a nonpatent stalklike attachment to the esophagus, and EPS with CCAM, is consistent with the concept of a shared etiology for BPFMs. Development of the alimentary and respiratory tract is regulated by a complex interaction of factors in time and space, and the development of the BPFMs appears to be related to a dysregulation of these developmental morphogens that include extracellular growth factors, proto-oncogenes, oncogenes, cytokines, cell adhesion molecules, and regulatory peptides [7,8]. In the current case, it could be hypothesized that the BPFM and teratoma shared a common etiology for dysregulated morphogens.…”

Section: E32mentioning

confidence: 78%

Congenital pulmonary malformations associated with esophageal duplication and teratoma: prenatal to postnatal management

Smith

Samuel

Lees

et al. 2008

Journal of Pediatric Surgery

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The lung and the gut: Common origins, close links

Cited by 23 publications

References 24 publications

Transient in utero disruption of Cystic Fibrosis Transmembrane Conductance Regulator causes phenotypic changes in Alveolar Type II cells in adult rats

Transient in utero disruption of Cystic Fibrosis Transmembrane Conductance Regulator causes phenotypic changes in Alveolar Type II cells in adult rats

Links Between Inflammatory Bowel Disease and Chronic Obstructive Pulmonary Disease

Congenital pulmonary malformations associated with esophageal duplication and teratoma: prenatal to postnatal management

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